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Editorial
February 24, 2015

Potential Hazards of Adding Nonsteroidal Anti-inflammatory Drugs to Antithrombotic Therapy After Myocardial Infarction: Time for More Than a Gut Check

Author Affiliations
  • 1Division of Cardiovascular Medicine, University of Tennessee–Chattanooga
  • 2Gill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky, Lexington
JAMA. 2015;313(8):801-802. doi:10.1001/jama.2015.0567

Nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandin and prostacyclin biosynthesis via their inhibition of cyclooxygenase (COX) enzymes. By inhibiting COX-1, aspirin reduces thromboxane production, and this leads to its antiplatelet effect. By more effectively inhibiting COX-2, other NSAIDs have relatively greater anti-inflammatory, antipyretic, and analgesic effects. The adverse effect profile of nonselective NSAIDs includes bleeding, particularly gastrointestinal bleeding, which is thought to result from gastric irritation, antiplatelet effects, and the loss of prostaglandin-mediated mucosal repair.1 Selective inhibitors of COX-2 were developed with the hope they would have fewer gastrointestinal adverse effects and would be highly effective against chronic inflammatory states, such as arthritis.

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